The role of ferroptosis in the pathogenesis and progression of endometriosis. History of the question and current evidence

Abstract

Endometriosis is a common gynaecological disease that affects about 10% of women of reproductive age — approximately 200 million people worldwide. It is characterised by the presence of endometrium-like tissue outside the uterine cavity. Endometriosis predominantly causes reproductive dysfunction, pelvic pain, dyspareunia, infertility, reduced quality of life and is accompanied by combined hyperplastic processes — uterine myoma, adenomyosis and others. According to our studies, hyperestrogenism plays a significant role in the pathogenesis of endometriosis, which allows us to consider it a hyperproliferative disease. The role of oxidative stress in the pathogenesis of various forms of endometriosis is among the topical and insufficiently studied problems. Cyclic changes in endometriosis foci, their enlargement and inflammation create a microenvironment with high iron content, reactive oxygen species and free radicals that promote adhesion and growth of ectopic endometrial cells. Based on which we developed an experimental model of endometriosis to further investigate the role of iron metabolism in the development and maintenance of endometriosis. It is suggested that the primary defect of endometriosis is an abnormal eutopic endometrium characterised by resistance to ferroptosis, a process of iron-mediated non-apoptotic programmed cell death. Currently, the pathogenesis of endometriosis and the role of oxidative stress and iron metabolism requires further study, which is of high relevance, practical and theoretical importance.